Atherosclerosis最新文献

{"title":"Transportation noise and the cardiometabolic risk.","authors":"Thomas Münzel, Marin Kuntic, Andreas Daiber, Mette Sørensen","doi":"10.1016/j.atherosclerosis.2025.119148","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.119148","url":null,"abstract":"<p><p>Transportation noise is a widespread and often underestimated environmental pollutant, posing a substantial health risk particularly in urban areas. In contrast to air pollution, the health effects of noise pollution are less extensively documented. Defined as an unwanted and/or harmful sound, noise pollution affects over 20 % of the European Union (EU) population, contributing to an estimated 12,000 premature deaths and 48,000 new cases of ischemic heart disease annually. Recent epidemiological evidence strengthens the link between transportation noise and cardiovascular disease (CVD). A 2024 Umbrella + review with subsequent meta-analyses found that road traffic noise was associated with risk of CVD, more specifically a 4.1 % higher risk for ischemic heart disease, 4.6 % for stroke, and 4.4 % for heart failure per 10 dB(A). Translational and experimental studies have investigated the biological mechanisms behind noise-induced cardiovascular damage, showing that noise impacts stress and sleep pathways. Human studies reveal that nighttime noise impairs vascular function, elevates stress hormone levels, and triggers inflammation and oxidative stress, particularly in individuals with pre-existing CVD. Animal research corroborates these findings, demonstrating that noise exposure leads to endothelial dysfunction, elevated blood pressure, and oxidative stress through mechanisms shared with traditional cardiovascular risk factors. Mitigation strategies are crucial to reducing the health impacts of environmental noise. For road traffic, transitioning to electric vehicles offers minimal noise reduction, necessitating measures such as noise-reducing asphalt, low-noise tyres, and changes in urban infrastructure, whereas for aircraft noise nighttime flight bans and optimized flight paths are important tools for reducing noise exposure. Addressing co-exposure to noise and air pollution is essential for a comprehensive approach to mitigating the environmental burden on cardiovascular health.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"119148"},"PeriodicalIF":4.9,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The vicious circle of chronic kidney disease and hypertriglyceridemia: What is first, the hen or the egg?","authors":"Tramontano Daniele ,&nbsp;D'Erasmo Laura ,&nbsp;Larouche Miriam ,&nbsp;Brisson Diane ,&nbsp;Lauzière Alex ,&nbsp;Di Costanzo Alessia ,&nbsp;Bini Simone ,&nbsp;Minicocci Ilenia ,&nbsp;Covino Stella ,&nbsp;Baratta Francesco ,&nbsp;Pasquali Marzia ,&nbsp;Cerbelli Bruna ,&nbsp;Gaudet Daniel ,&nbsp;Arca Marcello","doi":"10.1016/j.atherosclerosis.2025.119146","DOIUrl":"10.1016/j.atherosclerosis.2025.119146","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is documented to cause alterations in lipid metabolism, and this was considered a potent driver of increased cardiovascular risk. Among the diverse alteration of lipid traits in CKD, research endeavours have predominantly concentrated on low-density lipoproteins (LDL) in view of the potent pro-atherogenic role of these lipoprotein particles and the demonstration of protective cardiovascular effect of reducing LDL. However, few studies have focused on the metabolism of triglyceride-rich lipoproteins and even fewer on their role in causing kidney damage. Therefore, the comprehensive description of the impact of hypertriglyceridemia (HTG) in CKD pathophysiology remains largely undetermined. This reflects the difficulty of disentangling the independent role of triglycerides (TG) in the complex, bidirectional relationship between TG and kidney disease. Abnormal neutral lipid accumulation in the intrarenal vasculature and renal cells eventually due to HTG may also promote glomerular injury, throughout mechanisms including oxidative stress, mitochondrial dysfunction and proinflammatory responses. While epidemiological and experimental evidence suggests a potential role of TG in kidney damage, the causal mechanisms and their clinical relevance remain unclear, representing a significant area for future investigation. This review aims to highlight the intricate interplay between TG metabolism and kidney disease, shedding light on the mechanisms through which HTG may influence kidney functionality.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119146"},"PeriodicalIF":4.9,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143579991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune checkpoint inhibitors: Unravelling atherosclerotic cardiovascular risk","authors":"Rhys Gray ,&nbsp;Charlotte Manisty ,&nbsp;Richard Cheng ,&nbsp;Amardeep Dastidar ,&nbsp;Mamas Mamas ,&nbsp;Arjun Ghosh","doi":"10.1016/j.atherosclerosis.2025.119147","DOIUrl":"10.1016/j.atherosclerosis.2025.119147","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119147"},"PeriodicalIF":4.9,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143549218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of bone morphogenetic protein 4 alleviates angiotensin II-induced abdominal aortic aneurysm by reducing inflammation and endothelial-mesenchymal transition","authors":"Yingzheng Weng ,&nbsp;Xihao Wang ,&nbsp;Yimin Tang ,&nbsp;Changqing Du ,&nbsp;Xinyao Li ,&nbsp;Kefu Zhu ,&nbsp;Yizhong Bao ,&nbsp;Wenping Zeng ,&nbsp;Changhong Cai ,&nbsp;Bingbing Jia ,&nbsp;Zhouxin Yang ,&nbsp;Lijiang Tang","doi":"10.1016/j.atherosclerosis.2025.119134","DOIUrl":"10.1016/j.atherosclerosis.2025.119134","url":null,"abstract":"<div><h3>Background and aims</h3><div>Abdominal aortic aneurysm (AAA) is one of the most common fatal macrovascular diseases worldwide which pathogenesis is still not well clarified. In this study, we systematically investigated the alternations of endothelial cell (ECs) functions and phenotypes by single-cell RNA sequencing in angiotensin (Ang) II-induced AAA mice models.</div></div><div><h3>Method and results</h3><div>According to 10 × single-cell sequencing analysis, we revealed that ECs inflammation and endothelial-mesenchymal transition (EndoMT) were involved in the progress of Ang II-induced AAA. Three types of ECs, including <em>Mature ECs</em> (uninjured ECs), <em>EndoMT ECs</em> and <em>Injury &amp; inflammation ECs</em> successively emerged during the progression of AAA. By using pseudotime-trajectory analysis, we speculated bone morphogenetic protein 4 (BMP4) as a candidate gene, participating in Ang II-induced AAA by regulating EndoMT and vascular inflammation. We found that inhibition of BMP4 ameliorated EndoMT and vascular inflammation in Ang II-induced AAA in vivo. In addition, we found that exogenous BMP4 directly promoted the phenotypic transition, inflammation, cell migration and invasion of mouse aortic endothelial cells via PI3K/AKT/mTOR pathways in vitro. Finally, Protein-protein interaction (PPI) analysis and co-immunoprecipitation (Co-IP) revealed that biglycan (BGN) directly combined with BMP4 and promoted the conversion of EndoMT.</div></div><div><h3>Conclusion</h3><div>Our findings firstly revealed a critical role of BMP4 in AAA progression, which promoted disease progression by inducing EndoMT and reprogramming ECs from anti-inflammatory to proinflammatory phenotype.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119134"},"PeriodicalIF":4.9,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143609760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Edgeworthia gardneri (Wall.) Meisn protects against HFD-induced murine atherosclerosis through improving gut microbiota-mediated intestinal barrier integrity","authors":"Le Tang ,&nbsp;Jiangsheng Li ,&nbsp;Mingxuan Luan ,&nbsp;Manman Qin ,&nbsp;Chao Zhong ,&nbsp;Yifeng Zhang ,&nbsp;Yanfei Xie ,&nbsp;Min Shi ,&nbsp;Liang Qiu ,&nbsp;Jun Yu","doi":"10.1016/j.atherosclerosis.2025.119132","DOIUrl":"10.1016/j.atherosclerosis.2025.119132","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Gut microbiota plays a crucial role in the development and progression of atherosclerosis. &lt;em&gt;Edgeworthia gardneri&lt;/em&gt; (Wall.) Meisn, a member of the Thymelaeaceae family and the &lt;em&gt;Edgeworthia&lt;/em&gt; genus, has been previously shown in our studies to attenuate atherogenesis when administered orally as an ethanolic extract (EEEG). However, the interaction between EEEG and gut microbiota, and the mechanism by which gut microbiota exerts anti-atherosclerotic effects, remains unclear.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Aims&lt;/h3&gt;&lt;div&gt;This study aims to determine whether the anti-atherosclerotic properties of EEEG are associated with gut microbiota remodeling.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Method&lt;/h3&gt;&lt;div&gt;Atherosclerosis was induced in &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; mice using a high-fat diet (HFD). The mice were treated with EEEG or Lactobacillus plantarum for 16 weeks. The composition of gut microbiota was analyzed through 16S rDNA sequencing. To assess whether the anti-atherosclerotic effects of EEEG depend on the gut microbiota, HFD-fed mice were treated with a cocktail of antibiotics or underwent fecal microbiota transplantation (FMT). Simultaneously, plaque areas in the aortic roots and whole aortas of apolipoprotein E deficient (&lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt;) mice were evaluated using oil red O staining and hematoxylin-eosin staining. Serum levels of LPS, fluorescein isothiocyanate-dextran, and expression levels of tight junction proteins were measured to identify the effects of EEEG on gut barrier dysfunction in HFD-fed &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; mice.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;The results revealed that EEEG treatment significantly reduced atherosclerotic lesions by ameliorating lipid accumulation and preserving gut barrier integrity. The protective effects were abrogated by antibiotics administration, concomitant with an increase in gut barrier permeability by decreasing expression of tight junction proteins. The microbial analysis indicated an augmented abundance of &lt;em&gt;Lactobacillus&lt;/em&gt;, &lt;em&gt;Turicibacter&lt;/em&gt;, &lt;em&gt;Faecalibacterium&lt;/em&gt;, &lt;em&gt;Akkermansia&lt;/em&gt;, and &lt;em&gt;Desulfovibrio&lt;/em&gt; following EEEG treatment. Meanwhile, transplantation of fecal microbiota from EEEG-treated mice exerted the anti-atherosclerotic effect in the high-fat diet (HFD)-fed &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; recipient mice, accompanied by improvement of gut barrier integrity through upregulation of tight junction protein expression. Furthermore, exogenous supplementation of &lt;em&gt;Lactobacillus plantarum&lt;/em&gt; mitigated AS in &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; mice and improved the gut epithelial barrier function by increasing the expression level of Zo-1.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;These results suggest that the anti-atherosclerotic efficacy of EEEG is attributed to the preservation of gut barrier integrity mediated by gut microbiota. EEEG and its enriched &lt;em&gt;Lactobacillus plantarum&lt;/em&gt; may be promising adjunct","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119132"},"PeriodicalIF":4.9,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Achieved levels of apolipoprotein B and plaque composition after acute coronary syndromes: Insights from HUYGENS","authors":"Masashi Fujino ,&nbsp;Giuseppe Di Giovanni ,&nbsp;Julie Butters Bhsc ,&nbsp;Yu Kataoka ,&nbsp;Thomas Hucko ,&nbsp;Adam J. Nelson ,&nbsp;Steven E. Nissen ,&nbsp;Peter J. Psaltis ,&nbsp;Stephen J. Nicholls","doi":"10.1016/j.atherosclerosis.2025.119145","DOIUrl":"10.1016/j.atherosclerosis.2025.119145","url":null,"abstract":"<div><h3>Background and aims</h3><div>Addition of the PCSK9 inhibitor, evolocumab, to statin therapy promoted coronary plaque stabilization after an acute coronary syndrome. While apolipoprotein B (ApoB) has been proposed as a goal for lipid-lowering therapy in the prevention of cardiovascular disease, its association with plaque stability has not been studied.</div></div><div><h3>Methods</h3><div>The High-Resolution Assessment of Coronary Plaques in a Global Evolocumab Randomized Study (HUYGENS) used serial optical coherence tomography to assess coronary plaque phenotypes in patients with non-ST elevation myocardial infarction treated with evolocumab plus statin or placebo plus statin for 52 weeks. Changes in plaque composition were studied in patients according to achievement of a goal ApoB level &lt;65 mg/dL.</div></div><div><h3>Results</h3><div>Of 112 patients, 67 (59.8 %) achieved the ApoB goal and had lower ApoB values at follow-up compared with those not at goal (37.1 ± 15.0 vs 92.7 ± 19.4 mg/dL, P &lt; 0.001). Patients achieving the ApoB goal demonstrated a greater increase in minimum fibrous cap thickness (+44.6 ± 36.0 vs +24.9 ± 38.1 μm, P = 0.007) and a more pronounced decrease in lipid arc (−57.8 ± 52.8 vs −27.0 ± 59.2°, P = 0.005) at follow-up, compared with those who did not achieve the ApoB goal. At follow-up, thin-cap fibroatheroma (TCFA) was less prevalent among patients achieving the ApoB goal compared with those not at goal (9.0 vs. 40.0 %, P &lt; 0.001). Multivariate analysis demonstrated that achieving an ApoB &lt;65 mg/dL at follow-up independently associated with the absence of TCFA at follow-up (P = 0.004).</div></div><div><h3>Conclusions</h3><div>Lower achieved ApoB levels associated with evidence of greater plaque stabilization even after controlling for low-density lipoprotein cholesterol levels. This highlights the importance of optimizing ApoB levels for the reduction of cardiovascular risk.</div></div><div><h3>Clinicaltrialsgov identifier</h3><div>NCT03570697.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119145"},"PeriodicalIF":4.9,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143510087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term body mass index trajectories and the risk of type 2 diabetes mellitus and atherosclerotic cardiovascular disease using healthcare data from UK Biobank participants","authors":"Anja Krüger ,&nbsp;Ko Willems van Dijk ,&nbsp;Diana van Heemst ,&nbsp;Raymond Noordam","doi":"10.1016/j.atherosclerosis.2025.119135","DOIUrl":"10.1016/j.atherosclerosis.2025.119135","url":null,"abstract":"<div><h3>Background and aims</h3><div>Most epidemiological studies ignore long-term burden, gain and variability in body weight in assessing cardiometabolic disease risk. We investigated the associations of body mass index (BMI) trajectories measured by general practitioners with incident type 2 diabetes (T2D) and coronary artery disease (CAD).</div></div><div><h3>Methods</h3><div>We used electronic healthcare data from 111,615 European-ancestry participants from UK Biobank (57.1 (SD 7.8) years, 59.6 % women) with at least three BMI measurements (median trajectory period: 14.9 [interquartile range 9.5, 20.1] years). We calculated six variables capturing different long-term aspects, including i.e. burden (long-term average, area under the curve), gain (slope) and variability (standard deviation, average of the [absolute] consecutive BMI differences). The variables were used in principal component (PC) analyses and k-means clustering. Newly-derived dimensions and subgroups were used as exposures in cox-proportional hazard models.</div></div><div><h3>Results</h3><div>The BMI-trajectory indices were captured in two PCs reflecting BMI burden and BMI gain. The BMI-burden PC associated with higher T2D (hazard ratio [95 % confidence interval] per SD higher PC: 1.57 [1.55,1.60]) and CAD (1.17 [1.15,1.19]) risks, while weak or no associations were observed with the BMI-gain PC (T2D: 1.03 [1.01,1.05]; CAD: 1.01 [0.98,1.03]). Participants with the highest BMI burden, compared to those with lowest BMI burden without significant gain, had highest T2D (6.96 [6.41,7.55]) and CAD (1.57 [1.45,1.69]) risks. Both methods to capture BMI burden, gain and variability showed superior model fit compared to a single baseline BMI assessment.</div></div><div><h3>Conclusions</h3><div>Long-term high BMI burden, irrespective of BMI gain, was a risk factor for cardiometabolic disease.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119135"},"PeriodicalIF":4.9,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic association of circulating lipids and lipid-lowering drug targets with vascular calcification","authors":"Pengfei Zhang ,&nbsp;Wenting Wang ,&nbsp;Qian Xu ,&nbsp;Jing Cui ,&nbsp;Mengmeng Zhu ,&nbsp;Yiwen Li ,&nbsp;Yanfei Liu ,&nbsp;Yue Liu","doi":"10.1016/j.atherosclerosis.2025.119136","DOIUrl":"10.1016/j.atherosclerosis.2025.119136","url":null,"abstract":"<div><h3>Background and aims</h3><div>Vascular calcification (VC) significantly increases the incidence and mortality of many diseases. The causal relationships of dyslipidaemia and lipid-lowering drug use with VC severity remain unclear. This study explores the genetic causal associations of different circulating lipids and lipid-lowering drug targets with coronary artery calcification (CAC) and abdominal aortic artery calcification (AAC).</div></div><div><h3>Methods</h3><div>We obtained single-nucleotide polymorphisms (SNPs) and expression quantitative trait loci (eQTLs) associated with seven circulating lipids and 13 lipid-lowering drug targets from publicly available genome-wide association studies and eQTL databases. Causal associations were investigated by univariable, multivariable, drug-target, and summary data-based Mendelian randomization (MR) analyses. Potential mediation effects of metabolic risk factors were evaluated.</div></div><div><h3>Results</h3><div>MR analysis revealed that genetic proxies for low-density lipoprotein cholesterol (LDL-C), triglycerides (TC) and Lipoprotein (a) (Lp(a)) were causally associated with CAC severity, and apolipoprotein B (apoB) level was causally associated with AAC severity. A significant association was detected between hepatic Lipoprotein(A) (<em>LPA</em>) gene expression and CAC severity. Colocalisation analysis supported the hypothesis that the association between <em>LPA</em> expression and CAC quantity is driven by different causal variant sites within the ±1 Mb flanking region of <em>LPA</em>. Serum calcium and phosphorus had causal associations with CAC severity.</div></div><div><h3>Conclusions</h3><div>Inhibitors targeting <em>LPA</em> might represent CAC drug candidates. Moreover, T2DM, hypercalcemia, and hyperphosphatemia are positively causally associated with CAC severity, while chronic kidney disease and estimated glomerular filtration rate are not.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119136"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of dietary fatty acids with the incidence of carotid atherosclerotic plaque components: A 6-year follow-up study with serial MRI","authors":"Luoshiyuan Zuo ,&nbsp;Maryam Kavousi ,&nbsp;Daniel Bos ,&nbsp;Trudy Voortman","doi":"10.1016/j.atherosclerosis.2025.119144","DOIUrl":"10.1016/j.atherosclerosis.2025.119144","url":null,"abstract":"<div><h3>Background and aims</h3><div>The influence of dietary fatty acids (FAs) on carotid atherosclerotic plaque components remains unknown. We aimed to assess the association of dietary saturated (SFA), mono-unsaturated (MUFA), and poly-unsaturated FAs (PUFA) with the incidence of carotid plaque components.</div></div><div><h3>Methods</h3><div>Within the population-based Rotterdam Study, 570 stroke-free participants (mean age: 68 years; 47 % women) with subclinical carotid atherosclerosis underwent two serial carotid MRI (mean scan interval: 5.9 years). Carotid calcification, lipid-rich necrotic core (LRNC) and intraplaque hemorrhage (IPH) were evaluated. Intake of dietary FAs was assessed by food-frequency questionnaires around the time of baseline MRI. We used generalized estimating equation to investigate the association between dietary FAs and new onset of carotid plaque components.</div></div><div><h3>Results</h3><div>We found that a higher PUFA intake was associated with a lower incidence of IPH (adjusted odds ratio (OR) per 5 g/d increase: 0.80 (95 % confidence interval (CI): 0.65 to 0.98)). In the substitution models, a modelled higher PUFA intake at the expense of MUFA or SFA was also associated with a lower risk of incident IPH, with adjusted ORs per 5 g/day more PUFA of 0.81 (95 % CI: 0.58 to 1.14) for replacing SFA and 0.60 (95 % CI: 0.37 to 0.97) for replacing MUFA. No associations between SFA or MUFA and the carotid plaque components were found.</div></div><div><h3>Conclusion</h3><div>Among persons with subclinical carotid plaque, dietary FA intake is a modifiable risk factor for changes in carotid plaque vulnerability. Diet with more PUFA is associated with a lower risk of IPH in carotid plaque.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119144"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of replacing sitting with standing and walking on cholesterol metabolism and inflammation in men and women who are overweight or obese","authors":"Willem Zwaan ,&nbsp;Bernard M.F.M. Duvivier ,&nbsp;Hans H.C.M. Savelberg,&nbsp;Herman E. Popeijus,&nbsp;Maurice C.J.M. Konings,&nbsp;Ronald P. Mensink,&nbsp;Jogchum Plat","doi":"10.1016/j.atherosclerosis.2025.119143","DOIUrl":"10.1016/j.atherosclerosis.2025.119143","url":null,"abstract":"<div><h3>Background and aims</h3><div>Reducing sedentary behaviour changes serum lipid and lipoprotein concentrations. However, detailed insights into effects on lipid and lipoprotein subclasses and functionalities, and markers of inflammation and endothelial dysfunction are lacking.</div></div><div><h3>Methods</h3><div>In this randomised cross-over study, 24 sedentary overweight/obese individuals followed two 4-day activity regimens under free-living conditions. The “Sit” regimen involved 13.5 h/day sitting, 1.4 h/day standing, and 0.7 h/day self-perceived light-intensity walking. During the “SitLess” regimen these activities lasted respectively 7.6, 4.0, and 4.3 h/day. Blood samples collected after each regimen were analysed for markers of lipid and lipoprotein metabolism, inflammation, and endothelial dysfunction.</div></div><div><h3>Results</h3><div>Compared to the Sit regimen, SitLess increased serum cholesterol concentrations in HDL (0.06 mmol/l, p = 0.002), large HDL A (0.05 mmol/l, p &lt; 0.001), medium HDL B (0.02 mmol/l, p &lt; 0.001) and small HDL C (0.09 mmol/l, p &lt; 0.001), LHDL particles concentrations (999 nmol/l, p &lt; 0.001) and HDL size (0.2 nm, p &lt; 0.001). ApoA-I, pro-ApoA-I, and HDL functionality remained unchanged. Triglyceride (−0.49 mmol/l, p &lt; 0.001), ApoB100 (−0.68 g/l, p = 0.007), and particle concentrations of LVLDL (−2.2 nmol/l, p = 0.002), SLDL (−58 nmol/l, p = 0.024) and LDL (−86 nmol/l, p = 0.006) decreased. Cholesterol concentrations in VLDL (−0.15 mmol/l, p &lt; 0.001), IDL (−0.11 mmol/l, p = 0.001) and small LDL C (−0.04 mmol/l, p &lt; 0.001) decreased, while large LDL A cholesterol (0.07 mmol/l, p = 0.031) and LDL particle size (0.1 nm, p = 0.004) increased. CRP concentrations (0.95 mg/dl, p = 0.003) rose.</div></div><div><h3>Conclusions</h3><div>Substituting sitting with standing and self-perceived light walking in free-living conditions, translates into lower CVD risk lipid and lipoprotein profiles in individuals who are overweight/obese. CRP significantly increased after the SitLess regimen.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119143"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}